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Computed tomographic angiography (CTA) was invented more than 20 years ago, but only gained acceptance recently, thanks to advancements in the computer technology. It can demonstrate areas of arterial stenosis or occlusion with accuracy nearly that of digital subtraction angiography (DSA). It is also able to clearly illustrate calcification, which is more difficult to define on magnetic resonance angiography and is not clearly depicted on DSA.Our retrospective study attempted to clarify the rate of occlusion or stenosis in the patients with acute ischemic stroke.Over the period of 7 months, 93 consecutive patients were admitted with acute ischemic stroke. Fifty-six patients underwent CTA and were included in this study. Most of the patients were admitted after 6 hours following onset of symptoms. There were 28 men and 28 women, and 80.4% of the cohort was of African-American origin. The majority of strokes were attributed to small-vessel disease (25/56). The rest of the cases were deemed secondary to atheroembolism (15/56), cardioembolism (9/56) or of unclear etiology (7/56). In 24 (42.9%) patients, CTA failed to reveal any abnormalities of the cerebrovascular tree. CTA demonstrated arterial occlusion in ten (17.9%) patients and stenosis of extracranial or intracranial arteries on the symptomatic side in 22 (39.2%) patients. There was very good correlation between CTA and ultrasound techniques (carotid duplex and transcranial Doppler). CTA was superior in demonstrating distal intracranial stenosis.Overall, CTA is an extremely valuable and fast way to emergently evaluate the cerebrovascular anatomy, making it very useful for pre-thrombolysis evaluation of patients with ischemic stroke.

Thrombotic thrombocytopenic purpura (TTP) is an extremely rare cause of status epilepticus. Review of literature demonstrated only four cases of brief status epilepticus (SE) associated with TTP. We describe a young woman with yet incomplete neurological recovery after prolonged refractory status epilepticus. Management required pentobarbital-induced coma for 60 days. Five months after onset, she was conversant and oriented with continued neuromuscular deficits. This is an unusual presentation of severe refractory SE associated with TTP. With aggressive life support and prolonged pentobarbital infusion, however, survival and the chance of meaningful recovery appear to be possible.

BACKGROUND Constriction of the sciatic nerve by loose ligation produces an inflammatory neuropathic injury. This represents an animal model for peripheral mononeuropathy. Oxygen-derived free radicals are suspected to play an important role in the pathogenesis of ischemia/reperfusion injury, leading to neurogenic inflammation. Hyperbaric oxygen (HBO) has been used anecdotally to treat clinically similar conditions in humans, but specific effects on the animal model have not been well studied. OBJECTIVE This study in a rat model examined the effects of hyperbaric oxygen on skin blood flow and tissue morphology by light and electron microscopy following sciatic nerve constriction. DESIGN A scientific investigation in a rat model. METHODS In this study, the neuropathic injury was established by loose ligation of the rat sciatic nerve. The animals were divided into three groups, sham (S, n=8), ligation but no treatment (LN, n=8) and ligation and treatment with hyperbaric oxygen (LT, n=8). The treatment group (n=8) received hyperbaric oxygen treatment immediately following the injury and daily for four additional days at the same time interval. One hundred percent O2 at 3 atmospheres absolute pressure (66 feet sea water) was administered for two hours. The hindpaws of the rats were observed by light microscopy, electron microscopy, laser Doppler flowmetry (LDF), and clinically for the presence of edema. RESULTS Untreated animals demonstrated marked tissue edema following sciatic constriction, whereas animals that received hyperbaric oxygen had minimal to no edema. The sham group demonstrated normal histology. The group not treated with hyperbaric oxygen demonstrated swollen mitochondria (2-3 times), with loss of cellular integrity, multiple vacuole formation in both nerve and muscle tissue, widened sarcomeres in muscle, and degenerative changes in the nerve myelin sheaths. The group treated with hyperbaric oxygen demonstrated preservation of cellular structure including mitochondrial integrity, no vacuole formation, and maintenance of normal, easily identifiable nerve structure. The sham group had no change of skin blood flow. Skin blood flow of LT group was decreased immediately after ligation (p

Dolichoectasia, or the dilation and increased curvature of intracranial vessels, has long been linked to atherosclerosis. Rather than the result of atheromatous alterations of the vessel wall, investigators now believe that the primary lesion is a defect in the internal elastic lamina and the elastic components of the media. Remodeled by shear and stress related to blood flow and turbulence, the thickened intima and lipid deposits are secondary phenomena. In some patients, dissection of the intracerebral vessel wall may be the initial event, and with the passage of time, dolichoectasia may be the final phase. We present two patients to illustrate the spectrum of changes that can involve the posterior circulation. The first patient had dolichoectasia of the basilar artery, and the second patient had dissection of the vertebral artery. Each patient died from diffuse subarachnoid hemorrhage, and each had a postmortem examination. To better understand the genetic mechanisms leading to smooth muscle and elastic fiber defects in dolichoectasia, we can focus on a subgroup of patients with polycystic kidney disease. This cohort of renal patients has an abnormally high frequency of intracranial aneurysms, hemorrhages, and dolichoectasia of intracranial vessels. Polycystin is the protein product of the gene PKD1, which undergoes mutation in autosomal dominant polycystic kidney disease. By studying the relationship between aberrant polycystin expression and vascular phenotype, we may someday understand the vascular abnormalities at the molecular level.

Dolichoectatic basilar artery has become a more frequent finding in patients examined with modern neuroimaging techniques. Described complications of basilar dolichoectasia include ischemic infarcts of the brainstem, compression of cranial nerves, and hydrocephalus. We describe a patient who initially presented with pontine ischemic infarct related to dolichoectatic basilar artery. Within several days of her admission, the patient died. Her basilar lesion ruptured, resulting in a devastating subarachnoid hemorrhage, a relatively rare and fatal complication of this condition. We postulate that any deterioration in a patient with dolichoectatic basilar artery should not be automatically attributed to infarct, and that hemorrhage should be considered too.

Cerebral vasospasm is a deadly complication following the rupture of intracranial aneurysms. The time course of cerebral vasospasm is unique in that it is slow developing, usually takes 4–7 days to peak, but lasts up to 2–3 weeks, and is resistant to most known vasodilators. These special features make cerebral vasospasm the most important determinant in the outcome of patients suffering subarachnoid hemorrhage. The available treatment strategies include mechanical dilation of spastic cerebral arteries (angioplasty) and non-selective vasodilatation such as by Ca 2+ channel blockers. One new development in the experimental treatment of cerebral vasospasm is the looming target of signaling pathways. Understanding vasospastic signals in cerebral arteries might offer a new avenue for selective treatment of cerebral vasospasm in the future.

One of the important histological changes in cerebral vasospasm after subarachnoid hemorrhage (SAH) is endothelial cell damage, which involves apoptosis. The current study was undertaken to determine whether anti-apoptosis therapy prevents apoptosis and reverses vasospasm in a dog SAH model. Twenty-three mongrel dogs of either sex, weighing 17–25 kg, were subjected to autologous arterial blood injection into the cisterna magna on day 0 and day 2, and sacrificed on day 7. Angiography was performed on day 0 before blood injection and on day 7 before sacrifice. Caspase-2 (Z-VDVAD-FMK, 10 μM) inhibitor, caspase-3 (Z-DEVD-FMK, 10 μM) inhibitor, or vehicle (DMSO) were injected intrathecally from day 2 to day 6. The effects of caspase inhibitors on apoptosis and vasospasm were evaluated by angiography and transmission electron microscopy. The residual diameter of the basilar artery on day 7 in SAH dogs without treatment was 53.4±5.5% of the day 0 diameter. Marked damage to the endothelial cells, including apoptotic like changes, was observed in these arteries. Both caspase inhibitors prevented apoptosis in the endothelial cells. Only caspase-3 inhibitor, however, had a near- significant effect on reducing 13.3% of angiographic vasospasm. Higher doses and early treatment, as well as other more potent apoptosis inhibitors, are recommended for future studies.

Cerebral vasospasm is a major cause of morbidity and mortality in patients suffering from subarachnoid hemorrhage (SAH). Despite numerous studies, the pathogenesis of this deadly disorder is not clearly understood. Alterations in endothelial cells are a distinct morphological feature of cerebral vasospasm and some recent studies suggest that apoptosis might play a role in the cells' death. The goal of the present study is to examine the time course of apoptosis in endothelial cells of spastic cerebral arteries following experimental subarachnoid hemorrhage. Fifteen dogs were used in the present study. Twelve of them were divided into three groups (four per group) and subjected to a double-hemorrhage method of SAH. Following SAH, groups were sacrificed respectively on days 3, 5, and 7. Three dogs served as controls without blood injection. The basilar arteries were studied with the transmission electron microscopy and with angiography. Angiographic vasospasm began on day 3 and peaked on day 7. In morphologic studies, control dogs did not demonstrate apoptotic-like changes in endothelial cells of the basilar arteries. Beginning with day 3, apoptotic-like changes were noted in endothelial cells and consisted of condensation of peripheral nuclear chromatin, blebbing of the cell membrane, and condensation of the cytoplasm. Such changes progressed with time and were maximally developed by day 7. This is the first study that demonstrates the time course of apoptotic-like changes in the endothelial cells in the vasospastic basilar artery. Apoptosis might play an important role in the pathogenesis of vasospasm.

The objective of the present study was to investigate if MAPK can be activated by a non-receptor agonist KCl, which depolarizes membrane to increase intracellular Ca(2+) and contracts cerebral arteries. Rabbit basilar arteries were used in isometric tension and western blot analysis studies. KCl produced a concentration-dependent contraction and an elevation of phospho-MAPK, which can be abolished by nicardipine, a voltage-dependent Ca(2+) channel blocker, and by PD98059 or U0126, MAPK kinase inhibitors. Thus, MAPK can be activated by the elevation of intracellular Ca(2+), independent of the activation of either G-protein coupled receptors or receptor tyrosine kinase. KCl which not only depolarizes membrane potentials, opens voltage-dependent Ca(2+), and increases intracellular Ca(2+), but also, probably by elevation of intracellular Ca(2+), triggers the activation of MAPK which seems responsible for a predominant part of the contraction of KCl in the rabbit basilar arteries.

Object. Mitogen-activated protein kinase (MAPK) may be involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage. This study was conducted to investigate the ability of the MAPK inhibitors PD98059 and U-0126 to reverse vasospasm in a double-hemorrhage model in dogs.Methods. Twenty-two adult mongrel dogs of either sex, each weighing 18 to 24 kg, were divided randomly into four groups: control SAH (four dogs), vehicle- (dimethyl sulfoxide, six dogs), PD-98059— (six dogs), and U-0126—treated groups (six dogs). The double-hemorrhage model was created by an autologous blood injection into the cisterna magna on Days 0 and 2. An intracisternal injection of MAPK inhibitors was administered once per day on Days 3 through 6. Cerebral angiography was performed on Days 0 and 7 before the animals were killed. Western blot analysis was used to study the effects of hemorrhage and drug treatment on the MAPK immunoprecipitation.Severe vasospasm developed in the dogs in the control and vehicle-treated groups (basilar artery [BA] diameter reduction 46.6 ± 5.5% and 49.3 ± 4.6%, respectively). In the PD-98059—treated group, most of the dogs developed mild vasospasm (18.9 ± 6.2%). In the U-0126—treated group, severe vasospasm was observed despite treatment (39.6 ± 6.4%). The PD-98059 but not the U-0126 abolished MAPK immunoprecipitation in the spastic BAs. However, treatment with either PD-98059 or U-0126 improved the clinical scores of the dogs.Conclusions. The present study is the first in which the effects of MAPK inhibitors on vasospasm have been investigated in vivo. The authors demonstrate that MAPK may play a role in vasospasm and that PD-98059 is a potential candidate for the treatment of cerebral vasospasm.

BACKGROUND Morphological presentations of cerebral vasospasm, such as dystrophy and desquamation of endothelial cells, corrugation of the internal elastic layer, and necrotic changes in smooth muscle cells, are well defined in large cerebral arteries. This study was undertaken to examine pathological changes in cerebral penetrating arteries in a canine double hemorrhage model. METHODS Eighteen mongrel dogs were subjected to an autologous arterial blood (0.4 mL/kg) injection into the cisterna magna on day 0 and day 2 after withdrawal of an equivalent amount of cerebrospinal fluid. Angiogram was performed on day 0 before the blood injection and on the day the dogs were sacrificed. The dogs were divided into four groups: control (day 0) (n = 4), hemorrhage and sacrificed on day 3 (n = 4), day 5 (n = 5), and day 7 (n = 5). The penetrating arteries were removed and found to be spastic on days 3, 5, and 7, but not in the control group. RESULTS Endothelial dystrophy and partial desquamation were recorded in all dogs sacrificed on days 5 and 7. Condensation of chromatin, blebbing of the membrane, and condensation of cytoplasm were identified in many endothelial cells, features that are consistent with apoptosis. The morphological changes in the penetrating arteries were more pronounced on days 5 and 7. CONCLUSIONS Vasospasm occurred in cerebral penetrating arteries in a canine double hemorrhage model. The morphological change in penetrating arteries, especially apoptosis in endothelial cells, is consistent with an early phase of vasospasm. Vasospasm in a penetrating artery may contribute to the cerebral ischemia that occurs during vasospasm.

BACKGROUND Vasospasm in the penetrating arteries contributes to ischemic neurological deficit. It may be as important as angiographic vasospasm because it would explain the discrepancies between angiographic vasospasm and clinical symptoms in some patients. It may also underlie the different effects of vasodilators. The present study examined this hypothesis by looking at the effect of the inhibitors of mitogen-activated protein kinase (MAPK) on vasospasm of the penetrating arteries. METHODS Twenty-two adult mongrel dogs of either sex were used for the dog double-hemorrhage model. The dogs were randomly divided into four groups: control-hemorrhage, vehicle-treated, PD98059-treated, and U0126-treated groups. The drug injections were started on Day 3 after the first subarachnoid hemorrhage (SAH). The clinical status of the dogs was studied, based on their activity, appetite, and focal neurological symptoms. On Day 7, all the dogs were sacrificed, and the penetrating arteries from the brain stem were prepared for transmission electron microscopy. RESULTS (1) Severe vasospasm developed in the basilar arteries in the SAH-without-treatment group (control), in the DMSO-treated group (DMSO), and in the U0126 treatment group with mean reduction of the basilar artery diameter of 46.57%, 49.3%, and 39.6%, respectively. In the PD98059-treatment group only a mild vasospasm was observed and the mean reduction of the basilar artery diameter was 18.9%. (2) All the dogs in the control SAH and vehicle-treated groups developed severe angiographic and clinical vasospasm. The penetrating arteries were contracted, and the endothelial and smooth muscle cells were dystrophic. (3) The dogs in the U0126-treated group developed severe angiographic, but not clinical, vasospasm. The penetrating arteries were not contracted, and the endothelial and smooth muscle cells were not dystrophic. (4) The dogs in the PD98059 group developed mild angiographic vasospasm. No dog developed clinical symptoms that could be attributed to vasospasm. In morphological studies, the penetrating arteries were slightly contracted, but the cells were not dystrophic. CONCLUSIONS Vasospasm of the penetrating arteries, but not angiographic vasospasm, is consistent with the clinical symptoms and signs of vasospasm. MAPK may be important in maintaining vasospasm of both major and penetrating cerebral arteries. The correlation of the improvement in the clinical score with the reduction of vasospasm in the penetrating arteries demonstrated an important role of penetrating arteries in the morbidity and mortality caused by SAH.

Background and Purpose —We have previously reported that extracellular ATP activates P 2u receptors and increases intracellular free Ca 2+ ([Ca 2+ ] i ) by G protein/phospholipase C/inositol 1,4,5-triphosphate pathways in cerebral artery smooth muscle cells. However, the possible contribution of other signaling pathways remains unclear. This study was undertaken to investigate the role of protein tyrosine kinase (PTK) and mitogen-activated protein kinase (MAPK) in mediating ATP-induced Ca 2+ mobilization in rat basilar artery smooth muscle cells (RBASMCs). Methods —RBASMCs were freshly isolated, and [Ca 2+ ] i was monitored by fura 2 microfluorimetry. MAPK phosphorylation was studied by the Western blot technique. Results —ATP produced a biphasic [Ca 2+ ] i response, which consists of releasing Ca 2+ from internal stores and influx from extracellular space. PTK inhibitors tyrphostin 51 and genistein inhibited [Ca 2+ ] i response to ATP. Tyrphostin A1, an inactive analogue of tyrphostins, failed to reduce the ATP-induced response. MAPK kinase inhibitor PD98059, but not U0126, reduced the ATP-induced [Ca 2+ ] i response. Phosphatidylinositol 3-kinase (PI3-K) tyrosine kinase inhibitor wortmannin, but not janus tyrosine kinase (JAK2) inhibitor AG490, partially inhibited the [Ca 2+ ] i response induced by ATP. In addition, ATP enhanced MAPK phosphorylation in a concentration- and time-dependent manner, and genistein, tyrphostin 51, PD98059, and U0126 inhibited MAPK phosphorylation. Conclusions —Extracellular ATP produced [Ca 2+ ] i elevation and MAPK phosphorylation in RBASMCs, and the effect was regulated by PTK. The role of MAPK in ATP-induced [Ca 2+ ] i elevation is not clear. PI3-K tyrosine kinase and JAK2 tyrosine kinase may not play an important role in the ATP-induced [Ca 2+ ] i response in RBASMCs.

BACKGROUND Cerebral vasospasm after subarachnoid hemorrhage is a prolonged contraction that leads to cerebral ischemia or infarction. Morphological studies of cerebral arteries during vasospasm have shown extensive necrosis of smooth-muscle cells and desquamation and dystrophy of endothelial cells. The mechanism of cellular death is unknown. METHODS We report an observation of apoptotic changes in the cerebral arteries of a patient who died after suffering severe cerebral vasospasm caused by aneurysmal rupture. Subarachnoid hemorrhage and cerebral vasospasm were confirmed by computed tomography scanning and angiogram. Histological and immunohistological examinations for apoptosis were performed in cerebral arteries. For control, the arteries from another patient, who died of trauma without head injury, were used. RESULTS Corrugation of the internal elastic lamina and increased amounts of connective tissue was demonstrated by light microscopy. Apoptotic changes, characterized by condensation of chromatin of the nucleus and detachment from the basal membrane, were found on transmission electron microscopy in endothelial cells. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling reaction revealed positive staining of the nuclei of the endothelial cells. CONCLUSIONS This study demonstrates that apoptosis occurred in the cerebral arteries in a patient who died of cerebral vasospasm. The possible role of apoptosis in cerebral vasospasm is discussed.

Object. Oxyhemoglobin (OxyHb) is one of the most important spasmogens for cerebral vasospasm that follows aneurysmal subarachnoid hemorrhage. The cytotoxic effect of OxyHb has been documented in endothelial and smooth-muscle cells; however, the pattern of cell death—necrosis or apoptosis—as the final stage of cell damage has not been demonstrated. This study was undertaken to determine if OxyHb induces apoptotic changes in cultured bovine aortic endothelial cells.Methods. Confluent bovine aortic endothelial cells were treated with OxyHb in a concentration- and time-dependent manner. Cell density was assayed by counting the number of cells that attached to culture dishes after exposure to OxyHb. To identify apoptotic changes, the investigators used three specific methods: DNA fragmentation (electrophoreses), the apoptotic body (transmission electron microscopy), and cleavage of poly (adenosine diphosphate ribose) polymerase (PARP [Western blotting]).Conclusions. Oxyhemoglobin decreased cell density in a concentration- and time-dependent manner. Analysis of DNA showed a pattern of internucleosomal cleavage characteristic of apoptosis (DNA ladder). Transmission electron microscopy demonstrated condensation of nuclei and apoptotic bodies in OxyHb-treated endothelial cells. Western blotting with the PARP antibody revealed that the 116-kD PARP was cleaved to the 85-kD apoptosis-related fragment. These results for the first time demonstrated that the OxyHb induces apoptosis in cultured endothelial cells.

The pathogenesis of cerebral vasospasm that follows aneurysmal subarachnoid hemorrhage (SAH) is poorly understood. Multiple methods have been used to clarify the mechanism of spasmogen-induced vasospasm, however, each method has its own limitations. Cultured cells lose their phenotype and inter-cellular interactions, and animal models are expensive and can be used only in some established centers. Isolated cerebral arteries have been used extensively to study the contractility by transient exposure to spasmogens that, however, can hardly represent cerebral vasospasm that occurs 2-4 days after SAH. In this study, we cultured arteries with bloody cerebrospinal fluid (CSF) from patients of cerebral vasospasm and studied the contractility of the arteries 1, 3 and 4 days later. This method preserves artery wall structure, prolongs exposure of artery to bloody CSF, and is simple and inexpensive. Cultured rat aorta showed enhanced contractile response to 5-HT (p < 0.001) but reduced response to KCl (p < 0.05) 4 days after culturing with bloody CSF. We concluded that the contractility of arteries was modified by prolonged incubation with bloody CSF. Our observations in this study could be important and may explain some aspects of pathogenesis of cerebral vasospasm.

Object. Mitogen-activated protein kinase (MAPK) is an important signaling factor in vascular proliferation and contraction, which are the two features of cerebral vasospasm that follow subarachnoid hemorrhage. The authors studied the possible involvement of MAPK in hemolysate-induced signal transduction and contraction in rabbit basilar artery (BA).Methods. Isometric tension was used to record the contractile response of rabbit BA to hemolysate, and Western blots were obtained using antibodies for MAPK.The following results are reported. 1) Hemolysate produced a concentration-dependent contraction of rabbit BA; however, preincubation of arteries with the MAPK kinase (MEK) inhibitor PD-98059 markedly reduced this contraction. The administration of PD-98059 also relaxed, in a concentration-dependent fashion, the sustained contraction induced by 10% hemolysate. 2) The Janus tyrosine kinase 2 inhibitor AG-490, preincubated with arterial rings, reduced the contractile response to hemolysate but failed to relax the sustained contraction induced by this agent. The Src-tyrosine kinase inhibitor damnacanthal and the phosphatidylinositol 3—kinase inhibitor wortmannin failed to reduce hemolysate-induced contraction. 3) Hemolysate produced a time-dependent elevation of MAPK immunoreactivity as seen on Western blots of rabbit BA. The MAPK was enhanced 1 minute after hemolysate exposure and the effect reached maximum levels at 5 minutes. The immunoreactivity of MAPK decayed slowly over time, but the level of this kinase was still higher than the basal level, even at 2 hours after exposure to hemolysate. Preincubation of arteries with the MEK inhibitor PD-98059 abolished the effect of hemolysate on MAPK immunoreactivity.Conclusions. Hemolysate produced contraction of rabbit BA, possibly by activation of MAPK, and therefore MAPK inhibitors may be useful in the treatment of cerebral vasospasm.

BACKGROUND Percutaneous transluminal angioplasty (PTA) dilates constricted arteries at the circle of Willis to reverse cerebral ischemia caused by cerebral vasospasm. Although 90% of the patients show angiographic improvement after PTA, only 70% show clinical improvement. Why some patients do not improve after PTA is unknown. We report on a 48-year-old woman who failed to improve after PTA and died from aneurysm rerupture. Pathologic studies were performed to determine why PTA failed to reverse the symptoms of cerebral ischemia. METHODS The arteries of the brain were studied by light microscopy using Gomori’s trichrome stain. The arteries were also studied by scanning and transmission electron microscopy. RESULTS The arteries that were dilated with PTA showed compression of the connective tissue, stretching of the internal elastic lamina, and a combination of compression and stretching of the smooth muscle. The small arteries and arterioles that had been treated with an infusion of intra-arterial papaverine were constricted with a thickened intimal layer. CONCLUSION The persistence of cerebral vasospasm in small and perforating arteries may contribute to the failure of cerebral ischemia to reverse after PTA.

In this study, we have reviewed our experience with anticoagulation-associated intraventricular hemorrhage (IVH). Our goal was to determine if IVH is also an independent prognosticator of fatal outcome in patients with anticoagulation-associated intracerebral hemorrhage (ICH).This study is a retrospective analysis of medical records and computed tomographic imaging. Eighty-eight patients with warfarin-associated ICH were analysed, including eight patients with predominant IVH.There was a very low rate of hemorrhage extension in patients with predominant IVH. Despite that, those patients had 50% 30 day mortality. Overall patients with ICH had 45% 30 day mortality. Ventricular extension raised mortality in ICH patients to 75%, while the absence of ventricular extension carried only 23% 30 day mortality. IVH was significantly associated with 30 day mortality (p0.001). Panventricular extension was uniformly fatal in patients with ICH and carried 75% 30 day mortality in patients with predominant IVH. On a multivariate logistic regression model including age, ICH volume and IVH, ICH volume (p0.001) and IVH (p = 0.003) remained independently associated with early mortality.Extension of anticoagulation-associated ICH into ventricular system caused a high mortality, especially in patients with panventricular involvement. IVH is an independent predictor of early death in these patients. In our experience, the majority of IVH do not expand over time and poor outcome appears to be related to the magnitude of the initial insult.

Acute bilateral acute carotid arteries occlusion is a very rare condition. We describe a patient with initial right middle cerebral artery syndrome who developed coma and quadriplegia 1 h after thrombolysis with intravenous tPA and was found to have bilateral cervical internal carotid artery occlusion.

Subarachnoid hemorrhage (SAH) resulting from the rupture of a cerebral aneurysm represents one major cause of stroke. SAH may be followed by a spontaneous severe contraction of major cerebral arteries, a condition referred to as cerebral vasospasm. Vasospasm may result in brain ischemia or actual tissue death. This constrictive vascular state is devastating, remains largely untreatable, and is a major cause of morbidity and mortality in SAH patients. Approximately 30,000 Americans are affected by this condition each year. The overall death rates are 25%, and significant neurological complications occur in 50% of individuals who survive the initial bleed. This report highlights some of the important aspects of this vascular disease. Anat. Rec. (New Anat.) 253:58-63, 1998. © 1998 Wiley-Liss, Inc.

OBJECTIVE To evaluate the validity of the FOUR (Full Outline of UnResponsiveness) score (ranging from 0 to 16), a new coma scale consisting of 4 components (eye response, motor response, brainstem reflexes, and respiration pattern), when used by the staff members of a medical intensive care unit (ICU). PATIENTS AND METHODS This interobserver agreement study prospectively evaluated the use of the FOUR score to describe the condition of 100 critically ill patients from May 1, 2007, to April 30, 2008. We compared the FOUR score to the Glasgow Coma Scale (GCS) score. For each patient, the FOUR score and the GCS score were determined by a randomly selected staff pair (nurse/fellow, nurse/consultant, fellow/fellow, or fellow/consultant). Pair wise weighted κ values were calculated for both scores for each observer pair. RESULTS The interrater agreement with the FOUR score was excellent (weighted κ: eye response, 0.96; motor response, 0.97; brainstem reflex, 0.98; respiration pattern, 1.00) and similar to that obtained with the GCS (weighted κ: eye response, 0.96; motor response, 0.97; verbal response, 0.98). In terms of the predictive power for poor neurologic outcome (Modified Rankin Scale score, 3-6), the area under the receiver operating characteristic curve was 0.75 for the FOUR score and 0.76 for the GCS score. The mortality rate for patients with the lowest FOUR score of 0 (89%) was higher than that for patients with the lowest GCS score of 3 (71%). CONCLUSION The interrater agreement of FOUR score results was excellent among medical intensivists. In contrast to the GCS, all components of the FOUR score can be rated even when patients have undergone intubation. The FOUR score is a good predictor of the prognosis of critically ill patients and has important advantages over the GCS in the ICU setting.

Deep vein thrombosis (DVT) is a risk factor for patients with acute stroke. Subclinical DVT is more common than clinically apparent DVT. DVT manifests with lower extremity swelling that might be associated with pain. Venous duplex ultrasound is a simple diagnostic procedure for detection of a DVT. However, as many as 30% of patients with acute pulmonary embolism show no evidence of lower extremity DVT, and thus a negative venous duplex ultrasound does not exclude the diagnosis of acute pulmonary embolism. Data suggest that heparin, of any type, may reduce the risk of venous thromboembolism in neurosurgical patients. One trial has shown that mechanical devices, such as intermittent pneumatic compression, significantly decrease the occurrence of asymptomatic DVT for patients with intracerebral hemorrhage as compared with elastic stockings alone, although this advantage was not found in a meta-analysis of prospective studies. Limitations in DVT prophylaxis raise a question about the need for more aggressive DVT surveillance.

Background and Purpose— Analyze the relationship between the location and extent of sinus thrombosis and presence and severity of brain lesions. Methods— Retrospective chart and neuroimaging review of patients with documented CVST. A CVST score was devised to quantify the extent of cerebral venous sinus thrombosis. Results— Nineteen of 56 (34%) patients had brain lesions. The extent of sinus thrombus was associated with increased risk of brain lesions (CVST score 1.9 among patients without brain lesions versus 3.1 in those with lesions; P =0.006). Age, sex, and acquired or hereditary thrombophilias were not associated with the risk of parenchymal lesions. Functional outcomes were favorable even in patients with extensive CVST and parenchymal lesions at presentation. Conclusions— The extent of the sinus involvement correlates with the risk of brain lesions in patients with CVST, but additional factors might also contribute to their occurrence.

Seizures may occur during or soon after rupture of an intracranial aneurysm. The use of antiepileptic drugs (AEDs) is a controversial issue. The overall conclusions from 2 recent studies in aneurysmal subarachnoid hemorrhage are that 1) many patients receive AEDs but should not; 2) long-term use is associated with worse outcome; and 3) short-term use is safer. Phenytoin may not be the first choice for seizure prophylaxis; newer AEDs such as levetiracetam might be more helpful in prevention and treatment of seizures.

Cerebral vasospasm is one of the major complications of subarachnoid hemorrhage. The delayed occurrence of this complication allows for preventive management and early therapeutic interventions. Yet, accurate and timely diagnosis remains challenging and therapeutic options are rather limited. This review discusses new developments in the diagnosis and medical management of cerebral vasospasm made possible by technological advances and growing understanding of the complex pathophysiology of this disorder. CT protocols including CT perfusion and MRI with diffusion and perfusion sequences are increasingly employed in the evaluation of patients with suspected vasospasm. These radiological studies can add important information to that provided by transcranial Doppler and conventional angiography. Nimodipine for the prevention of delayed functional sequelae and hemodynamic augmentation therapy for the treatment of symptomatic vasospasm remains the mainstay of medical management. Novel strategies under investigation include the use of endothelin receptor antagonists, magnesium sulphate and statins. The value of albumin is being formally studied in an ongoing trial. Interventions to enhance nitric oxide may prove viable in the near future.

Background Reinitiating warfarin sodium therapy in a patient with a recent warfarin-related intracerebral hemorrhage (WAICH) is a difficult clinical decision. Therefore, it is important to assess the outcome of resumption or discontinuation of warfarin therapy after WAICH. Objective To compare patients who survived an episode of WAICH and restarted warfarin therapy with a group of WAICH patients who did not resume warfarin therapy. Design, Setting, and Patients We conducted a follow-up study from November 1, 2001, through December 31, 2005, in a cohort from a single center. Long-term outcome was assessed at last clinical follow-up or via questionnaire. Main Outcome Measures Recurrent WAICH and thromboembolic events. Results Fifty-two patients were discharged from the hospital after a diagnosis of WAICH. Four patients were lost to follow-up. Mean follow-up among all patients was 43 (range, 1-108) months. Of the 23 patients who restarted warfarin therapy, 1 had a recurrent nontraumatic WAICH, 2 had traumatic intracerebral hemorrhages, and 2 had major extracranial hemorrhages. Of the 25 patients who did not restart warfarin therapy, 3 had a thromboembolic stroke, 1 had a pulmonary embolus, and 1 had a distal arterial embolus. Conclusions Restarting warfarin therapy in patients with a recent WAICH is associated with a low risk of recurrence, but patients are subjected to known, substantial risks of warfarin use. Withholding warfarin therapy is associated with a risk of thromboembolization.

Background Intracerebral hemorrhage (ICH) associated with warfarin sodium therapy is becoming more common as the use of this medication increases in the aging population. Objective To delineate factors associated with early mortality, determine variables responsible for poor functional outcome, and evaluate possible reasons for expansion of hemorrhage and associated parenchymal edema. Design Retrospective study of clinical and radiologic information for 88 patients with warfarin-associated ICH. Setting A single hospital. Patients Eighty-eight consecutive patients with warfarin-associated ICH. Methods Patients were included if the international normalized ratio (INR) at presentation with ICH was 1.5 or greater. Computed tomographic scans were reviewed for volumetric analysis of hematoma and perihematomal edema volume. Outcome variables included 7-day mortality, hematoma enlargement, and functional outcome based on the modified Rankin Scale score. Results Seven-day mortality (39.8%) was associated with a lower Glasgow Coma Scale sum score and larger ICH volume at presentation. Univariate analysis revealed that a lower Glasgow Coma Score sum score, larger initial ICH volume, higher initial and 48-hour maximum glucose concentrations, and higher percentage of ICH expansion were significantly associated with poor functional outcome at hospital discharge. At multivariate analysis, only Glasgow Coma Score and ICH volume remained significantly associated with functional outcome measured at hospital discharge and at the last follow-up visit. Conversely, INR at presentation, time to INR correction, initial blood pressure, and enlargement of edema were not associated with functional outcome either at hospital discharge or at the last follow-up. Neither serum glucose concentration at admission nor highest level during the first 48 hours had any correlation with ICH or parenchymal edema enlargement. In addition, neither initial INR nor time to INR correction correlated with expansion of ICH or parenchymal edema. Conclusions Lower level of consciousness at presentation and larger initial ICH volume predict poor prognosis in patients with warfarin-associated ICH. In our study population, INR at presentation was not associated with functional outcome.

A subset of patients with major cerebral hemispheric ischemia due to distal internal carotid artery or proximal middle cerebral artery occlusion has rapid spontaneous improvement of neurologic deficits. This phenomenon has been designated the "spectacular shrinking deficit." A 79-year-old woman had the sudden onset of neurologic deficits consistent with a large right middle cerebral artery territory infarct. Serial multimodality imaging studies documented distal propagation and fragmentation of a proximal middle cerebral artery thrombus coinciding with rapid clinical improvement. Spectacular shrinking deficit provides a unique insight into the underlying characteristics of a patient population not treated with thrombolytics with impressive recovery from major hemispheric ischemia.

An 18-year-old man with anaplastic oligoastrocytoma was pronounced brain dead based on absent confounding factors, absent brainstem reflexes, apnea with CO2 challenge, and isoelectric EEG. Plantar flexion, triple flexion response, and …

The potential causes of acquired macroglossia are extensive. The authors report two cases of subacute marked tongue swelling resulting in airway compromise in patients with refractory status epilepticus requiring prolonged pentobarbital coma. The hospitalization histories of the reported patients were retrospectively reviewed. The tongue swelling completely resolved in one case and significantly improved in the other after discontinuation of pentobarbital infusion or switching to phenobarbital. The authors speculate that the causes were multifarious, likely a combination of localized angioedema due to barbiturate vehicle and triggered by an initial tongue bite. Progressive tongue swelling causing airway obstruction can occur well beyond the acute phase of status epilepticus and may potentially cause problems with extubation in nontracheotomized patients.

Background: Amyloidosis is an uncommon disorder that ultimately leads to fatal multiorgan failure. Ischemic strokes have been sporadically described but are not well characterized. The purpose of this study was to review the pathophysiologic relationship between primary systemic amyloidosis and ischemic stroke, and to determine how often stroke is the first defining manifestation. Methods: Retrospective study of 49 patients with confirmed primary amyloidosis and ischemic stroke. All included patients had biopsy proven amyloidosis. Results: Forty patients were included in the study. Ischemic strokes occurred in 13 patients (32.5%) as the initial presentation of amyloidosis. Patients with initial stroke presentation had the worst outcome, with average survival of 6.9 months after established diagnosis with amyloidosis; strokes developed 9.6 months before diagnosis with primary amyloidosis. Thirty-seven percent experienced recurrent ischemic stroke. The majority (70%) of patients had cardioembolic infarctions. Conclusions: Ischemic stroke is an underappreciated complication of primary amyloidosis. In the absence of obvious clinical and cardiogenic manifestations, primary amyloidosis should be considered when echocardiography demonstrates thickening of the valves, restrictive pattern, and increased echogenicity. Ischemic strokes as an initial presentation of primary amyloidosis carries a worse prognosis.

Subarachnoid hemorrhages caused by intracranial dissections are rare. The management of dissections in these cases not clear.Case report.An 82-year-old woman presented with acute drowsiness and vomiting. CT scan demonstrated extensive subarachnoid hemorrhage and hydrocephalus that subsequently required placement of ventriculoperitoneal shunt. Angiography revealed extensive basilar artery dissection and no aneurysms. The dissection did not produce a critical stenosis and, taking into consideration that the patient had a previous occlusion of her distal left vertebral artery, it was decided to manage the patient conservatively. On a 3-month follow-up, the patient was free of recurrent events.Basilar artery dissection can present with subarachnoid hemorrhage. No guidelines are available for management of basilar artery dissections and treatment should be tailored to the individual patient.

We describe a case of the patient with multiple contraindications for thrombolysis who underwent successful mechanical embolectomy for occlusion of the right carotid terminus. Her pre-procedural NIHSS was 16.The patient demonstrated remarkable recovery within an hour of the procedure, and this clinical improvement was sustained at followup.This case illustrates that mechanical embolectomy is a safe and potentially very effective intervention to treat major intracranial vessel occlusions in patients with multiple contraindications for thrombolysis.

The signaling pathways of endothelin-1-induced contraction, including the role of protein tyrosine kinase (PTK), mitogen-activated protein kinase (MAPK), protein kinase C (PKC) and RhoA/Rho-kinase were studied using rabbit basilar arteries by isometric tension and Western blot. The following results were observed: (1) endothelin-1 produced phosphorylation of MAPK and RhoA and contraction by activation of endothelin-A but not endothelin-B receptors; (2) MAPK inhibitors, PD 98059 and U0126, PTK inhibitor, genistein, Src kinase inhibitor, damnacanthal, and Janus tyrosine kinase (JAK 2 ) inhibitor, AG-490, abolished endothelin-1-induced contraction and MAPK immunoreactivity; (3) PTK inhibitor, staurosporine, and phosphatidylinositol 3-kinase (PI-3K) inhibitor wortmannin abolished endothelin-1 induced contraction but not MAPK immunoreactivity; (4) Rho-kinase inhibitor, Y-27632, reduced endothelin-1-induced contraction; (5) PI-3K inhibitor, wortmannin, but not PKC and PTK inhibitors, reduced endothelin-1-induced RhoA activation; (6) endothelin-1 increased the level of myosin light chain (MLC) phosphorylation, and Rho-kinase inhibitor, Y-27632, reduced the effect of endothelia1 on MLC phosphorylation. This study demonstrated that three signaling pathways Src-JAK 2 -PTK-MAPK, PI-3K-RhoA-Rhokinase-MLC and PKC all contribute to endothelin-1-induced contraction in the rabbit basilar artery. MAPK is downstream of PTK, Src and JAK pathways. PI-3 kinase and MLC might be the upstream and downstream factors of RhoA activation.

This preliminary study was undertaken to explore the possible protective effect of caspase inhibitors Z-VDVAD-FMK and Z-DEVD-FMK in apoptosis and vasospasm in penetrating arteries during cerebral vasospasm. Experimental subarachnoid hemorrhage (SAH) was induced in 16 dogs by an intracisternal injection of autologous arterial blood (0.4 ml/kg) on Day 0 and Day 2. The dogs were then randomly divided into four groups: control-SAH, vehicle-control, and two treatment groups. In the treatment groups, caspase inhibitors (10 microM) were intracisternally injected each day beginning on Day 2 until Day 6. Effects of the inhibitors were analyzed utilizing angiography, the clinical status of the dogs (activity, appetite, and neurological deficits), and transmission electron microscopy of the penetrating arteries. All the dogs were sacrificed on Day 7. In control-SAH and vehicle-control groups, severe angiographic vasospasm, poor clinical status, and penetrating vasospasm were registered in all the dogs. In the treatment groups, all the dogs developed angiographic vasospasm and vasospasm in penetrating arteries, however, with benign clinical statues. The occurrence of apoptosis in endothelial cells was reduced by caspase-2 but not by caspase-3 inhibitor. Caspase inhibitors failed to prevent vasospasm either in major or in penetrating arteries. The improvement of clinical scores by the caspase inhibitors may be related to their protection of the endothelial cells. Further investigations using more rigorous clinical scoring system and quantitative information on the degree of apoptosis in the vessels, as well as in the brain parenchyma are recommended.

This study was undertaken to investigate the role of p44/42 MAPK in a dog double hemorrhage model of subarachnoid hemorrhage (SAH), and whether MEK inhibitors can alter the degree of SAH-induced vasoconstriction. The diameter of the basilar artery, which was compared with day 0 angiogram, decreased gradually in a time-dependent manner from day 3 (80%), day 5 (68%) through day 7 (53.5%). The level of MAPK (p44/42) immunoprecipitation peaked on day 3 and remained enhanced through day 7 (P < 0.05). MEK inhibitor PD98059 significantly reduced p44/42 MAPK immunoprecipitation and significantly reversed vasospasm and increased residual diameter to 79.0% on day 7. These results demonstrated that p44/42 MAPK kinase is involved in the pathogenesis of cerebral vasospasm. The MEK inhibitor PD98059 might be useful in the treatment of vasospasm.

Confluent rat aortic smooth muscle cells were treated with OxyHb in a concentration- and time-dependent manner. A high concentration of OxyHb (100 μM) within 24 h decreased cell density. DNA analysis showed a smear pattern characteristic of cell necrosis. Transmission electron microscopy demonstrated disintegration of the cell membrane and destruction of cell organelles. Western blotting using PARP antibody revealed that 116 kDa PARP was not cleaved to 85 kDa, an apoptosis-related fragment. On the contrary, a low concentration of OxyHb (10 μM) produced apoptotic cell death at 72 h that was supported by DNA analysis and TUNEL staining. These results demonstrated that a high level of OxyHb induced necrosis within 24 h and a low concentration of OxyHb produced apoptosis after 72 h in cultured smooth muscle cells. Morphological alterations induced by OxyHb might contribute to the vascular wall changes in the cerebral arteries following subarachnoid hemorrhage (SAH).

Background and Purpose —It has been suggested that mitogen-activated protein kinase (MAPK) is involved in cerebral vasospasm after subarachnoid hemorrhage. The present study was undertaken to explore the inhibitory effect of U0126, a novel MAPK inhibitor, in the contraction of the rabbit basilar artery by 3 spasmogens: hemolysate, oxyhemoglobin, and bloody cerebrospinal fluid (CSF) from patients with vasospasm. Methods —The contraction and relaxation of rabbit basilar arteries were measured by isometric tension. MAPK immunoprecipitation was assessed by Western blot analysis. Results —(1) Pretreatment of the rabbit basilar arteries with U0126 reduced contractions to hemolysate, oxyhemoglobin, or bloody CSF applied subsequently. (2) In the absence of endothelial cells, U0126 produced an inhibitory effect similar to the contractions induced by hemolysate, oxyhemoglobin, or bloody CSF. (3) U0126 relaxed the sustained contraction induced by hemolysate, oxyhemoglobin, or bloody CSF. (4) Hemolysate, oxyhemoglobin, and bloody CSF enhanced MAPK immunoprecipitation. (5) U0126 reduced MAPK immunoprecipitation induced by hemolysate, oxyhemoglobin, and bloody CSF. (6) Hemolysate, oxyhemoglobin, and bloody CSF significantly increased MAPK activity in the rabbit basilar artery. (7) U0126 abolished the effect of hemolysate, oxyhemoglobin, or bloody CSF on MAPK activation. Conclusions —This study demonstrated a role of MAPK in the contraction of rabbit basilar arteries by hemolysate, oxyhemoglobin, and bloody CSF. MAPK inhibitor U0126 may be useful in the treatment of cerebral vasospasm.

We hypothesize that the mechanism of cerebral vasospasm after subarachnoid hemorrhage may not be a delayed and prolonged vascular response to certain spasmogens but a more complicated cascade, including contraction, cell death, and proliferation. This study was undertaken to demonstrate the apoptotic cell death induced by oxyhemoglobin in cultured endothelial cells in vitro, apoptosis in endothelium in vivo in a canine double hemorrhage model of experimental subarachnoid hemorrhage, and apoptosis in cerebral endothelial cells in a patient who died of cerebral vasospasm. (1) Oxyhemoglobin-produced endothelial apoptotic cell was demonstrated by apoptotic bodies [transmission electron microscopy (TEM)] and DNA ladders. (2) Endothelial cell damage and detachment were observed in dog middle cerebral arteries 5 days after blood injection. (3) In a patient who died 20 days after aneurysmal subarachnoid hemorrahge, endothelial detachment and apoptotic endothelial cells were demonstrated by TEM and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) reaction. These studies demonstrated that apoptosis may be an important step in vasospasm development. They opened a new avenue for treatment of vasospasm.

It has been suggested that tyrosine kinases are involved in smooth muscle contraction [1] induced by hemolysate or other spasmogens and might be involved in cerebral vasospasm. Mitogen-activated protein kinase (MAPK), a tyrosine kinase substrate, was activated by oxyhemoglobin (OxyHb) [5] and hemolysate [9] and contributed to cerebral arterial contraction. MAPK inhibitor PD98059 reduced the contraction of a rabbit basilar artery by hemolysate [9] and endothelin-1 [8].

Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a combination of prolonged contraction and vessel remodeling that may lead to cerebral ischemia or infarction [2]. Morphological studies of cerebral arteries affected by vasospasm often show extensive necrosis of smooth-muscle cells [1] as well as desquamation and dystrophy of endothelial cells [7, 11]. The actual mechanisms of cellular death following cerebral vasospasm are not known. Recent studies of post-SAH vasospasm in this laboratory strongly suggest that endothelial cells may be dying through apoptotic pathways [8, 10].

Many extracellular stimuli (including growth factors, hormones, stress, elevated temperature and G-protein coupled receptor agonists) initialize the phosphorylation cascades leading to the activation of mitogen-activated protein kinase (p44/42 MAPK) [2]. p44/42 MAPK activation may lead to an expression of the early genes, such as c-jun or c-fos, thus leading to the cellular proliferation [3]. p44/42 MAPK can cause the phosphorylation of caldesmon, thus promoting prolonged contraction [1]. It has been reported in several in vitro studies that p44/42 MAPK is involved in the prolonged contraction of the cerebral arteries, caused by hemolysate [8] and endothelin-1 [9], the most important causative agents for vasospasm. The levels of c-fos, and c-jun were increased in the presence of hemolysate, reaching maximum expression between 30 and 60 minutes in rat aorta smooth muscle cells [7].

Endothelin-1 (ET-1), a potent vascular smooth muscle constrictor, is one of the possible spasmogens in cerebral vasospasm. However, the role of ET-1 in non-muscle compaction (another aspect of the pathogenesis of cerebral vasospasm) has not been reported. This study was undertaken to demonstrate the effect of ET-1, as well as erythrocyte lysate and bloody cerebrospinal fluid (CSF), on fibroblast populated collagen lattice (FPCL) compaction. Human dermal fibroblasts were used to form FPCL. The concentration-dependent effect of ET-1 was examined in the absence and presence of an ETA receptor antagonist (BQ-485), or an ETB receptor antagonist (BQ-788), or both. FPCL compaction was determined by measuring reduction of areas over five days following treatment. To compare the effect of ET-1 on lattice compaction, erythrocyte lysate and bloody CSF obtained from a cerebral vasospasm patient were also tested. We found that ET-1 increased FPCL compaction in a concentration-dependent (but not time-dependent) manner. Erythrocyte lysate produced the strongest compaction, however, without time-dependence. Bloody CSF promoted FPCL compaction in a time-dependent fashion. Compaction induced by ET-1 was inhibited by BQ-485 but not by BQ-788. We concluded that ET-1 promotes FPCL compaction by activation of ETA receptors. Other components in bloody CSF or erythrocytes may also contribute to FPCL compaction.

BACKGROUND Post-traumatic vasospasm is a well-recognized sequela of head injury. The risk factors associated with post-traumatic vasospasm have not been well defined. We studied 119 consecutive patients with head injury to determine the risk factors for post-traumatic vasospasm. METHODS Twenty-nine (27.1%) patients were excluded from the study because of poor insonation (n = 12) or a hospital stay of less than 72 hours (n = 17). Seventy (77.8%) of 90 patients suffered severe head injury. Sixteen (17.8%) patients sustained moderate head injury and four (4.4%) patients sustained mild head injury. All patients were monitored with transcranial Doppler (TCD) ultrasonography daily. RESULTS Post-traumatic vasospasm was detected in 32 (35.6%) of 90 patients. Among these patients, 29 (90.6%) had severe head injury, and three (9.4%) had moderate head injury. None of the patients with mild head injury suffered post-traumatic vasospasm. In most cases, the onset of post-traumatic vasospasm began on the fifth day and lasted 1 to 9 days. In 8 (25%) patients, post-traumatic vasospasm began within the first three days of the head injury. Among 32 patients with post-traumatic vasospasm, 10 (31.2%) patients had mild vasospasm, 20 (65.5%) had moderate vasospasm, and 2 (6.3%) had severe post-traumatic vasospasm. Clinical deterioration was documented in two (2.5%) patients. CONCLUSIONS Development of post-traumatic vasospasm correlated only with severe subarachnoid hemorrhage on initial computed tomographic scan. There was an increased incidence of post-traumatic vasospasm in patients with epidural hematomas, subdural hematomas, and intracerebral hemorrhages. The Glasgow Coma Scale (GCS) score on admission was inversely related to the development of post-traumatic vasospasm. In most cases, the period of vasospasm was short and clinical deterioration was rare. Probably, two varieties of post-traumatic vasospasm exist, one that lasts a shorter time and does not correlate with the presence of SAH, and a second that correlates with the presence of SAH, lasts longer, and resembles aneurysmal vasospasm.

Object. Myonecrosis in the tunica media, which is defined morphologically, is one of the most striking alterations in the cerebral arterial wall following subarachnoid hemorrhage (SAH). In this study, oxyhemoglobin (OxyHb) was added to cultured rat aortic smooth muscle cells to determine the pattern of cell death by morphological and biochemical techniques.